Posts tagged obesity
Articles and news from the latest research reports.
A new study by University of North Carolina School of Medicine pediatrics researchers finds a surprising difference in the eating habits of overweight children between ages 9 and 17 years compared to those younger than 9.
Younger children who are overweight or obese consume more calories per day than their healthy weight peers. But among older overweight children the pattern is reversed: They actually consume fewer calories per day than their healthy weight peers.
How to explain such a seemingly counterintuitive finding?
“Children who are overweight tend to remain overweight,” said Asheley Cockrell Skinner, PhD, assistant professor of pediatrics at UNC and lead author of the study published online Sept. 10, 2012 by the journal Pediatrics.
“So, for many children, obesity may begin by eating more in early childhood. Then as they get older, they continue to be obese without eating any more than their healthy weight peers,” Skinner said. “One reason this makes sense is because we know overweight children are less active than healthy weight kids. Additionally, this is in line with other research that obesity is not a simple matter of overweight people eating more — the body is complex in how it reacts to amount of food eaten and amount of activity.”
When psychology trumps anti-obesity drugs
Patients who fail to lose weight while taking anti-obesity drugs do so because of their beliefs about themselves and about the difficulty of losing weight.
That is the conclusion of research presented by Dr Amelia Hollywood from the University of Surrey at the Annual Conference of the British Psychological Society’s Division of Health Psychology. The conference is being held at the Holiday Inn in Liverpool from 5-7 September 2012.
Dr Hollywood interviewed 10 people, who had put on weight over the 18 months after they were prescribed the weight-loss medication Orlistat, about their experiences.
Dr Hollywood and her colleague Dr Jane Ogden found that the women attributed their failure to lose weight to the mechanics of the drug. They highlighted the barriers to weight loss and talked about other weight-loss methods that had not worked for them.
Overall, the researchers found, these people saw their failure to lose weight as an inevitable part of their identity. They felt that it reflected their self-fulfilling belief that they would be perpetual dieters.
Obesity and Metabolic Syndrome Associated With Impaired Brain Function in Adolescents
ScienceDaily (Sep. 3, 2012) — A new study by researchers at NYU School of Medicine reveals for the first time that metabolic syndrome (MetS) is associated with cognitive and brain impairments in adolescents and calls for pediatricians to take this into account when considering the early treatment of childhood obesity.
The study, funded by the National Institutes of Health under award number DK083537, and in part by award number 1ULIRR029892, from the National Center for Research Resources, appears online September 3 in Pediatrics.
As childhood obesity has increased in the U.S., so has the prevalence of metabolic syndrome — a constellation of three or more of five defined health problems, including abdominal obesity, low HDL (good cholesterol), high triglycerides, high blood pressure and pre-diabetic insulin resistance. Lead investigator Antonio Convit, MD, professor of psychiatry and medicine at NYU School of Medicine and a member of the Nathan Kline Research Institute, and colleagues have shown previously that metabolic syndrome has been linked to neurocognitive impairments in adults, but this association was generally thought to be a long-term effect of poor metabolism. Now, the research team has revealed even worse brain impairments in adolescents with metabolic syndrome, a group absent of clinically-manifest vascular disease and likely shorter duration of poor metabolism.
"The prevalence of MetS parallels the rise in childhood obesity," Dr. Convit said. "There are huge numbers of people out there who have problems with their weight. If those problems persist long enough, they will lead to the development of MetS and diabetes. As yet, there has been very little information available about what happens to the brain in the setting of obesity and MetS and before diabetes onset in children."
Daily or “circadian” rhythms including the sleep wake cycle, and rhythms in hormone release are controlled by a molecular clock that is present in every cell of the human body. This human clock has its own inbuilt, default rhythm of almost exactly 24 hours that allows it to stay finely tuned to the daily cycle generated by the rotation of Earth. This beautiful symmetry between the human clock and the daily cycle of Earth’s rotation is disrupted by exposure to artificial light cycles, and by irregular meal, work and sleep times. This mismatch between the natural circadian rhythms of our bodies and the environment is called “circadian desynchrony.”
“Electric light allowed humans to override an ancient synchronization between the rhythm of the human clock and the environment, and over the last century, daily rhythms in meal, sleep and working times have gradually disappeared from our lives … The human clock struggles to remain tuned to our highly irregular lifestyles, and I believe that this causes metabolic and other health problems, and makes us more likely to become obese." - Dr. Cathy Wyse (Chronobiology research group, University of Aberdeen)
Scientists find switch in the brain that could cause psychosis and addiction for cannabis users
(Source: Daily Mail)
Deep Brain Stimulation to Treat Obesity?
ScienceDaily (Aug. 20, 2012) — Scientific advances in understanding the “addiction circuitry” of the brain may lead to effective treatment for obesity using deep brain stimulation (DBS), according to a review article in the August issue of Neurosurgery, official journal of the Congress of Neurological Surgeons.
Electrical brain stimulation targeting the “dysregulated reward circuitry” could make DBS — already an accepted treatment for Parkinson’s disease — a new option for the difficult-to-treat problem of obesity. Dr. Alexander Taghva of Ohio State University and University of Southern California was lead author of the new review.
New Insights into ‘Reward Circuitry’
Obesity is a major public health problem that is notoriously difficult to treat. Although various approaches can promote weight loss, patients typically gain weight soon after the end of treatment. Drug options have shown limited success, with several products removed from the market because of serious adverse effects. Bariatric surgery is effective in many cases of obesity but has a significant failure rate and is associated with side effects.
Drug treatments for obesity have targeted the homeostatic (self-regulating) mechanism regulating appetite and body weight. The homeostatic mechanism is thought to involve the “feeding center” in the hypothalamus, which produces hormones (such as leptin and insulin) that affect feeding behavior.
Initial experiments exploring DBS as a treatment for obesity have targeted the hypothalamus. However — as with drug options focusing on the homeostatic mechanisms — success has been limited.
Possible Role of DBS for Obesity
More recent studies have explored a different mechanism: specifically, the “reward circuitry,” of the brain. Research has suggested that obesity is associated with a “relative imbalance” of the reward circuitry. Studies show that obese subjects — like those with addictive behaviors — are more impulsive and less able to delay gratification. The reward circuitry is intimately interconnected with the homeostatic mechanisms.
Together, these studies raise the possibility of new DBS approaches to the treatment of obesity. In DBS, a small electrode is surgically placed in a precise location in the brain. A mild electrical current is delivered to stimulate that area of the brain, with the goal of interrupting abnormal activity. Deep brain stimulation has become a standard and effective treatment for movement disorders such as Parkinson’s disease.
Just as stimulation of the brain areas responsible for abnormal movement helps “turn off” tremors in patients with Parkinson’s disease, stimulation of the areas involved in dysregulated reward circuitry might be able to “turn off” abnormal feeding behaviors in obese patients. The authors outline evidence implicating several different brain areas involved in the brain’s reward circuitry — particularly the “frontostriatal circuitry” — which could be useful targets for DBS.
Previous reports in individual patients have suggested that DBS performed for other reasons — particularly severe obsessive-compulsive disorder — have unexpectedly had unpredicted beneficial effects on addictive behaviors like smoking and overeating. Dr. Taghva and colleagues hope their review will open the way to further exploration of DBS as part of new and effective strategies for the treatment of obesity, perhaps in combination with therapies targeting the homeostatic mechanism.
Source: Science Daily
Molecular Link Between Circadian Clock Disturbances and Inflammatory Diseases Discovered
ScienceDaily (Aug. 1, 2012) — Scientists have known for some time that throwing off the body’s circadian rhythm can negatively affect body chemistry. In fact, workers whose sleep-wake cycles are disrupted by night shifts are more susceptible to chronic inflammatory diseases such as diabetes, obesity and cancer.
Researchers at the Salk Institute for Biological Studies have now found a possible molecular link between circadian rhythm disturbances and an increased inflammatory response. In a study published July 9 in Proceedings of the National Academy of Sciences, the Salk team found that the absence of a key circadian clock component called cryptochrome (CRY) leads to the activation of a signaling system that elevates levels of inflammatory molecules in the body.
"There is compelling evidence that low-grade, constant inflammation could be the underlying cause of chronic diseases such as diabetes, obesity and cancer," says senior author Inder Verma, a professor in Salk’s Laboratory of Genetics and the Irwin and Joan Jacobs Chair in Exemplary Life Science. "Our results strongly indicate that an arrhythmic clock system, induced by the absence of CRY proteins, alone is sufficient to increase the stress level of cells, leading to the constant expression of inflammatory proteins and causing low-grade, chronic inflammation."
Cryptochrome serves as a break to slow the circadian clock’s activity, signaling our biological systems to wind down each evening. In the morning, CRY stops inhibiting the clock’s activity, helping our physiology ramp up for the coming day.
To gain insight into the role of circadian clock components on immune function, the Salk scientists measured the expression of inflammatory mediators in the hypothalamus (the area of the brain responsible for sleep-wake cycle regulation) of mice with deleted CRY genes. Through a variety of tests, these knockout mice showed a significant increase in the expression of certain inflammatory proteins known as cytokines, including interleukin-6 and tumor necrosis factor-α, compared to mice with CRY genes.
"Our findings demonstrate that a lack of cryptochrome activates these proinflammatory molecules, indicating a potential role for cryptochrome in the regulation of inflammatory cytokine expression," says Satchidananda Panda, an associate professor in Salk’s Regulatory Biology Laboratory and one of the senior authors of the study.
In addition, the researchers found that a lack of CRY activated the NF-kB pathway, a molecular signaling conduit that controls many genes involved in inflammation. NF-kB is a protein complex in a cell’s cytoplasm, “just happily doing nothing,” says Verma. In response to stimuli, it is transferred to the cell’s nucleus, where it binds to inflammation genes and turns them on. The regulation of these genes is tightly controlled, but NF-kB does not completely shut off their expression. This lingering expression causes inflammation.
"Every time this pathway is turned on, there is a residual amount of inflammation left in the body," says Rajesh Narasimamurthy, a research associate in Verma’s laboratory and the paper’s first author. "That adds up over time, contributing to inflammation-related diseases like obesity and diabetes."
Previous research has shown that suppressing the activity of the NF-kB pathway might be a suitable therapy for some diseases. For example, NF-kB is activated automatically in cancer cells of multiple myeloma, which affects infection-fighting plasma cells in the bone marrow and allows the cells to proliferate. Drugs that inhibit this activity might be able to degrade NF-kB to the point that it may kill off the disease.
The researchers say the goal now is to find out how to suppress NF-kB activation in the short term to treat diseases like diabetes. They caution that any long-term suppression of the pathway could lead to chronic infection. “We would like to find molecules that modify this activity and focus on those small-molecule inhibitors to treat disease,” Verma adds.
Source: Science Daily
Opioid Receptors as a Drug Target for Stopping Obesity
ScienceDaily (July 31, 2012) — New research demonstrates that blocking the delta opioid receptor in mice created resistance to weight gain and stimulated gene expression promoting non-shivering thermogenesis.
Imagine eating all of the sugar and fat that you want without gaining a pound. Thanks to new research published in The FASEB Journal, the day may come when this is not too far from reality. That’s because researchers from the United States and Europe have found that blocking one of three opioid receptors in your body could turn your penchant for sweets and fried treats into a weight loss strategy that actually works. By blocking the delta opioid receptor, or DOR, mice reduced their body weight despite being fed a diet high in fat and sugar. The scientists believe that the deletion of the DOR gene in mice stimulated the expression of other genes in brown adipose tissue that promoted thermogenesis.
"Our study provided further evidence that opioid receptors can control the metabolic response to diets high in fat and sugar, and raise the possibility that these gene products (or their respective pathways) can be targeted specifically to treat excess weight and obesity," said Traci A. Czyzyk, Ph.D., a researcher involved in the work from the Department of Physiology at the Mayo Clinic in Scottsdale, Arizona.
Scientists studied mice lacking the delta opioid receptor (DOR KO) and wild type (WT) control mice who were fed an energy dense diet (HED), high in fat and sugar, for three months. They found that DOR KO mice had a lean phenotype specifically when they were fed the HED. While WT mice gained significant weight and fat mass on this diet, DOR KO mice remained lean even though they consumed more food. Researchers then sought to determine how DOR might regulate energy balance and found that DOR KO mice were able to maintain their energy expenditure levels, in part, due to an increase in non-shivering thermogenesis. This was evidenced by an increase in thermogenesis-promoting genes in brown adipose tissue, an increase in body surface temperature near major brown adipose tissue depots, and the ability of DOR KO mice to maintain higher core body temperatures in response to being in a cold environment.
"Don’t reach for the ice cream and doughnuts just yet," said Gerald Weissmann, M.D., Editor-in-Chief of The FASEB Journal. “We don’t know how all this works in humans, and of course, a diet of junk food causes other health problems. This exciting research identifies genes that activate brown adipose tissue to increase our burning of calories from any source. It may lead to a safe diet pill in the future.”
Source: Science Daily
Obese Kids as Bright as Thinner Peers
ScienceDaily (July 12, 2012) — Obesity is not to blame for poor educational performance, according to early findings from research funded by the Economic and Social Research Council (ESRC). In a study that combines statistical methods with genetic information, researchers dispel the false idea that being overweight has damaging educational consequences.
Previous studies have shown that children who are heavier are less likely to do well at school. However, Dr Stephanie von Hinke Kessler Scholder from University of York argues it’s vital to understand what drives this association. “We sought to test whether obesity ‘directly’ hinders performance due to bullying or health problems, or whether kids who are obese do less well because of other factors that are associated with both obesity and lower exam results, such as coming from a disadvantaged family,” Dr Scholder explains.
Researchers examined data on almost 4,000 members of the Children of the 90s Birth Cohort Study. These data include the children’s DNA. It is well known that genes are randomly allocated within a population, irrespective of factors such as socio-economic position. The researchers combined the latest developments from genetic epidemiology with statistical methodologies in economic and econometric research. Using two carefully chosen ‘genetic markers’, the research team was able to identify children with a slightly higher genetic pre-disposition to obesity.
“Based on a simple correlation between children’s obesity as measured by their fat mass and their exam results, we found that heavier children did do slightly worse in school,” Dr Scholder points out. “But, when we used children’s genetic markers to account for potentially other factors, we found no evidence that obesity causally affects exam results. So, we conclude that obesity is not a major factor affecting children’s educational outcomes.”
These findings suggest that the previously found negative relationship between weight and educational performance is driven by factors that affect both weight and educational attainment. Future research should focus on other determinants of poor educational outcomes, such as social class or a family’s socio-economic circumstances, Dr Scholder points out.
The finding that obesity is not a cause of poorer educational performance is, the researchers suggest, a positive thing. “Clearly there are reasons why there are differences in educational outcomes, but our research shows that obesity is not one of them,” Dr Scholder argues.
Source: Science Daily
How a protein meal tells your brain you are full
July 5, 2012
Feeling full involves more than just the uncomfortable sensation that your waistband is getting tight. Investigators reporting online on July 5th in the Cell Press journal Cell have now mapped out the signals that travel between your gut and your brain to generate the feeling of satiety after eating a protein-rich meal. Understanding this back and forth loop between the brain and gut may pave the way for future approaches in the treatment and/or prevention of obesity.
Feeling full involves more than just the uncomfortable sensation that your waistband is getting tight. Investigators reporting online on July 5th in the Cell Press journal Cell have now mapped out the signals that travel between your gut and your brain to generate the feeling of satiety after eating a protein-rich meal. Understanding this back and forth loop between the brain and gut may pave the way for future approaches in the treatment and/or prevention of obesity. Credit: Duraffourd et al., Cell
Food intake can be modulated through mu-opioid receptors (MORs, which also bind morphine) on nerves found in the walls of the portal vein, the major blood vessel that drains blood from the gut. Specifically, stimulating the receptors enhances food intake, while blocking them suppresses intake. Investigators have now found that peptides, the products of digested dietary proteins, block MORs, curbing appetite. The peptides send signals to the brain that are then transmitted back to the gut to stimulate the intestine to release glucose, suppressing the desire to eat.
Mice that were genetically engineered to lack MORs did not carry out this release of glucose, nor did they show signs of ‘feeling full’, after eating high-protein foods. Giving them MOR stimulators or inhibitors did not affect their food intake, unlike normal mice.
Because MORs are also present in the neurons lining the walls of the portal vein in humans, the mechanisms uncovered here may also take place in people.
"These findings explain the satiety effect of dietary protein, which is a long-known but unexplained phenomenon,” says senior author Dr. Gilles Mithieux of the Université de Lyon, in France. “They provide a novel understanding of the control of food intake and of hunger sensations, which may offer novel approaches to treat obesity in the future,” he adds.
Provided by Cell Press
Source: medicalxpress.com